Bipedalism and the dawn of uterine fibroids.

The high prevalence and burden of uterine fibroids in women raises questions about the origin of these benign growths. Here, we propose that fibroids should be understood in the context of human evolution, specifically the advent of bipedal locomotion in the hominin lineage. Over the ≥7 million years since our arboreal ancestors left their trees, skeletal adaptations ensued, affecting the pelvis, limbs, hands, and feet. By 3.2 million years ago, our ancestors were fully bipedal. A key evolutionary advantage of bipedalism was the freedom to use hands to carry and prepare food and create and use tools which, in turn, led to further evolutionary changes such as brain enlargement (encephalization), including a dramatic increase in the size of the neocortex. Pelvic realignment resulted in narrowing and transformation of the birth canal from a simple cylinder to a convoluted structure with misaligned pelvic inlet, mid-pelvis, and pelvic outlet planes. Neonatal head circumference has increased, greatly complicating parturition in early and modern humans, up to and including our own species. To overcome the so-called obstetric dilemma provoked by bipedal locomotion and encephalization, various compensatory adaptations have occurred affecting human neonatal development. These include adaptations limiting neonatal size, namely altricial birth (delivery of infants at an early neurodevelopmental stage, relative to other primates) and mid-gestation skeletal growth deceleration. Another key adaptation was hyperplasia of the myometrium, specifically the neomyometrium (the outer two-thirds of the myometrium, corresponding to 90% of the uterine musculature), allowing the uterus to more forcefully push the baby through the pelvis during a lengthy parturition. We propose that this hyperplasia of smooth muscle tissue set the stage for highly prevalent uterine fibroids. These fibroids are therefore a consequence of the obstetric dilemma and, ultimately, of the evolution of bipedalism in our hominin ancestors.

History of uterine artery occlusion and subsequent pregnancy.

OBJECTIVE: During mature placenta formation, select fetal trophoblasts invade maternal decidual arterioles and junctional zone arteries and change them into low-resistance uteroplacental arteries. Consequently, physicians performing vascular procedures that occlude the uterine arteries should understand their effects on miscarriage rates, the various toxemias of pregnancy, gross and microscopic placental anatomy, and invasive placentation. Thus, the objective of this article is to review the effects of vascular occlusion on pregnancy. CONCLUSION: In the long run, placental abnormalities may be the canary in the mine shaft to globally judge the effect of uterine artery embolization on pregnancy.

Are fibroids that become endocavitary after uterine artery embolization necessarily a complication?

OBJECTIVE: This commentary deals with the study by Verma et al. discussing submucosal and endocavitary fibroids after uterine artery embolization (UAE). CONCLUSION: UAE can infarct fibroids. Fibroids spontaneously infarct after childbirth. Because the postpartum cervix is patulous, infarcted fibroids that fall into the uterine cavity easily exit the uterus. Each patient contemplating UAE should anticipate that infarcted fibroids bordering on or inside the uterine cavity may require cervical dilatation or hysteroscopic resection for removal. The addition of either of these two gynecology procedures should not necessarily be regarded as a UAE complication or treatment failure.

Uterine artery occlusion: what is the evidence?

Symptomatic uterine fibroids are a relatively common gynecologic condition. In the past, fibroids were exclusively treated by myomectomy and/or hysterectomy. With the advent of uterine artery embolization or uterine artery occlusion, there now exist minimally invasive approaches to fibroid therapy especially for women in whom surgery is contraindicated or for those who wish to retain their uterus and possibly fertility. Fertility and pregnancy outcomes after these minimally invasive therapies are currently being evaluated.

Childbirth and myoma treatment by uterine artery occlusion: do they share a common biology?

When the uterine arteries are bilaterally occluded, either by uterine artery embolization or by laparoscopic obstruction, women with myomas experience symptomatic relief. After the uterine arteries are occluded, most blood stops flowing in myometrial arteries and veins, and the uterus becomes ischemic. It is postulated that myomas are killed by the same process that kills trophoblasts: transient uterine ischemia. When the uterine arteries are bilaterally occluded, either by uterine artery embolization (UAE) or by laparoscopic obstruction, women with myomas experience symptomatic relief. After the uterine arteries are occluded, most blood stops flowing in myometrial arteries and veins, and the uterus becomes ischemic. Over time, stagnant blood in these arteries and veins clots. Then, tiny collateral arteries in the broad ligament (including communicating arteries from the ovarian arteries) open, causing clot within myometrium to lyse and the uterus to reperfuse. Myomas, however, do not survive this period of ischemia. This is unique organ response to clot formation and ischemia. What allows the uterus to survive a relatively long period of ischemia while myomas perish? Childbirth appears to be the predicate biology. Following placental separation, the uteroplacental arteries and the draining veins of the placenta are torn apart at their bases in the junctional zone of the myometrium and bleed directly into the uterine cavity. Left unchecked, every woman would bleed to death in less than 10 minutes after placental delivery. Most women do not bleed to death because vessels in the uterus clot after placental delivery. During pregnancy, clotting and lytic factors in blood increase many fold. Following delivery, uterine contractions continue, intermittently, periodically slowing the velocity of flowing blood through myometrium. The combination of slowed blood flow, elevated clotting proteins, and torn placental vessels (known as Virchow's triad) causes blood in myometrial arteries and veins to clot. Fibrinolytic enzymes later lyse clot in arteries and veins not associated with placenta perfusion, and the uterus is reperfused. Remnant placental tissue - primarily uteroplacental arteries and veins - does not survive this period of ischemia. Placental tissue dies and over weeks is sloughed into the uterine cavity. At the same time, residual endometrial tissue grows under the sloughing placental tissue thus re-establishing the endometrial lining. It is postulated that myomas are killed by the same process that kills trophoblasts - transient uterine ischemia.